Evidence map›Paper›PMID 27132234›Full record

ReviewNaunyn-Schmiedeberg's archives of pharmacology2016

Pharmacological treatment options for mast cell activation disease.

Gerhard J Molderings, Britta Haenisch, Stefan Brettner, Jürgen Homann, Markus Menzen, Franz Ludwig Dumoulin, Jens Panse, Joseph Butterfield, Lawrence B Afrin

Open access · hybridAbstract readReview
In one paragraph

Review in Naunyn-Schmiedeberg's archives of pharmacology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers.

0numbers the graph read from it
0cells of the map it votes in
41citing papers in PubMed
2.8field-weighted citation impact, top 10% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

41 citing papers in PubMed, 73 citations in OpenAlex.

  1. Article
  2. Article
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  4. Characteristics and outcomes of patients with pediatric-onset non-mastocytosis mast cell activation disorders: A CEREMAST study.Pediatric allergy and immunology : official publication of the European Society of Pediatric Allergy and Immunology · 2026
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

9 authors at 7 institutions in 2 countries.

Gerhard J MolderingsInstitute of Human Genetics, University Hospital of Bonn, Sigmund-Freud-Strasse 25, 53127, Bonn, Germany. molderings@uni-bonn.de.
Britta HaenischGerman Center for Neurodegenerative Diseases (DZNE), Bonn, Germany.
Stefan BrettnerDepartment of Oncology, Hematology and Palliative Care, Kreiskrankenhaus Waldbröl, Waldbröl, Germany.
Jürgen HomannAllgemeine Innere Medizin, Gastroenterologie und Diabetologie, Gemeinschaftskrankenhaus, Bonn, Germany.
Markus MenzenAllgemeine Innere Medizin, Gastroenterologie und Diabetologie, Gemeinschaftskrankenhaus, Bonn, Germany.
Franz Ludwig DumoulinAllgemeine Innere Medizin, Gastroenterologie und Diabetologie, Gemeinschaftskrankenhaus, Bonn, Germany.
Jens PanseDepartment of Hematology, Oncology and Stem Cell Transplantation, Medical Faculty, RWTH Aachen University, Aachen, Germany.
Joseph ButterfieldProgram for the Study of Mast Cell and Eosinophil Disorders, Mayo Clinic, Rochester, MN, 55905, USA.
Lawrence B AfrinDivision of Hematology, Oncology, and Transplantation, University of Minnesota, Minneapolis, MN, 55455, USA.
Gemeinschaftskrankenhaus Havelhöhe · DEGerman Center for Neurodegenerative Diseases · DEKrankenhaus Waldfriede · DEMayo Clinic · USRWTH Aachen University · DEUniversity Hospital Bonn · DEUniversity of Minnesota Medical Center · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Mast cell activation disease (MCAD) is a term referring to a heterogeneous group of disorders characterized by aberrant release of variable subsets of mast cell (MC) mediators together with accumulation of either morphologically altered and immunohistochemically identifiable mutated MCs due to MC proliferation (systemic mastocytosis [SM] and MC leukemia [MCL]) or morphologically ordinary MCs due to decreased apoptosis (MC activation syndrome [MCAS] and well-differentiated SM). Clinical signs and symptoms in MCAD vary depending on disease subtype and result from excessive mediator release by MCs and, in aggressive forms, from organ failure related to MC infiltration. In most cases, treatment of MCAD is directed primarily at controlling the symptoms associated with MC mediator release. In advanced forms, such as aggressive SM and MCL, agents targeting MC proliferation such as kinase inhibitors may be provided. Targeted therapies aimed at blocking mutant protein variants and/or downstream signaling pathways are currently being developed. Other targets, such as specific surface antigens expressed on neoplastic MCs, might be considered for the development of future therapies. Since clinicians are often underprepared to evaluate, diagnose, and effectively treat this clinically heterogeneous disease, we seek to familiarize clinicians with MCAD and review current and future treatment approaches.

Indexed as

AnimalsAntineoplastic AgentsApoptosisCell DegranulationCell ProliferationHistamine AntagonistsHumansImmunosuppressive AgentsLeukemia, Mast-CellMast CellsMastocytosis, SystemicMolecular Targeted TherapyTreatment OutcomeAntineoplastic AgentsHistamine AntagonistsImmunosuppressive AgentsMast cellMast cell activation diseaseSystemic mast cell activation syndromeSystemic mastocytosisTherapy

Identifiers

PMID27132234
PMCPMC4903110
OpenAlexW2345273276

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.